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Role of Mononuclear Cells of IgA Nephropathy on ICAM-1 Expression in Mesangial Cells

OBJECTIVES: To investigate the possible role of mononuclear cells and their products in the pathogenesis of IgA nephropathy, in vitro expression of ICAM-1 on cultured mouse mesangial cell(MC) was examined after stimulation with mononuclear cell culture supernatant from patients with IgA nephropathy....

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Detalles Bibliográficos
Autores principales: Lee, Tae-Won, Park, Jai-Kyung, Ahn, Jae-Hyung, Ihm, Chun-Gyoo, Kim, Myung-Jae
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Association of Internal Medicine 1998
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531937/
https://www.ncbi.nlm.nih.gov/pubmed/9538628
http://dx.doi.org/10.3904/kjim.1998.13.1.27
Descripción
Sumario:OBJECTIVES: To investigate the possible role of mononuclear cells and their products in the pathogenesis of IgA nephropathy, in vitro expression of ICAM-1 on cultured mouse mesangial cell(MC) was examined after stimulation with mononuclear cell culture supernatant from patients with IgA nephropathy. METHODS: Peripheral blood mononuclear cells (PBMC) were isolated and cultured from 18 patients with primary IgA nephropathy, 8 normal controls and 5 patients with non-IgA nephropathy (FSGS 1, MGN 3, MPGN 1). ICAM-1 expression on cultured mouse MC by TNF-α, IL-1β and culture supernants of PBMC were analyzed using a cell ELISA method. The concentration of IL-1β and TNF-α in culture supernatants was measured by using a commercially available radioimmunoassay kit. RESULTS: Addition of human recombinant TNF-α induced an increased ICAM-1 expression in a dose-dependent manner. The expression of ICAM-1 was further increased after co-stimulation with TNF-α and IL-1β. Addition of PBMC culture supernatants into mouse MC induced significantly higher expression of ICAM-1 by supernatants from the patients with IgA nephropathy compared with that from normal controls. The concentration of TNF-α and IL-1β in supernatants from the patients with IgA nephropathy was significantly higher than that from those with non-IgA nephropathy. CONCLUSION: TNF-α and IL-1 released from mononuclear cells induced the up-regulation of ICAM-1 expression and this may be related to the immune pathogenesis of IgA nephropathy.